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Growth of Alzheimer Plaque Observed in Real Time
> 2/11/2008 3:09:18 PM

The tragedy of Alzheimer's Disease (AD) has spurred thousands of researchers into action, but while their efforts have added to our understanding, we still cannot even be sure of what causes AD. The predominant hypothesis is that excess amyloid-beta accretes into a plaque that disrupts neural function. Until now, this hypothesis could not be confirmed because amyloid plaques were only observed after autopsy; it was obvious that many patients with AD symptoms had plaques at the end of their lives, but the timing and the causation were unclear. A study by Dr. Melanie Meyer-Luehmann in the most recent issue of Nature clarifies the sequence of events.

Previous AD researchers bred lines of mice for vulnerability to amyloid plaques and cognitive decline. Dr. Meyer-Luehmann used these mice, but instead of examining them after-the-fact in an autopsy, she used an innovative imaging method called multiphoton confocal microscopy. This method. which involves replacing sections of the skull with glass and then scanning through them with lasers, enabled her to view plaque formation as it happened. Laser observation revealed that plaques form incredibly quickly� in as little as 24 hours.

The growth of plaques in one day is incredible because AD is usually envisioned as a slow degeneration, and sufferers often last many years before total breakdown. In addition to this startling discovery, researchers found that the order of events clearly went from neural plaque to immune cell reaction to neural disruption to cognitive impairment. Shortly after neural plaques form, the surrounding neurons distort into spirals. This strongly supports the idea that plaques cause cognitive defects. However, the MIT Technology Review cites a scientist with moderate skepticism. Dr. Steven Finkbeiner, associate director of the Gladstone Institute of Neurological Disease, praises the study and does not dispute that the ordering does imply some causation, but he questions whether the observed neural distortion can cause all of the symptoms associated with AD. It is also unclear whether mouse models are perfectly analogous to human patients.

The etiology of AD retains some mystery, but this latest study goes far towards resolving the chain of events that leads to dementia and death. As imaging techniques advance, we will hopefully see many more studies that track the precise way that our brains break down. Once we clearly see the timing and order of the damage, we will be much better equipped to put things back together.

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